At a central thermointegrative level, fever is a consequence of elevation of the homeostatic temperature set point within the hypothalamus. The posterior hypothalamus discriminates a difference between the set point and core body temperature. It then activates the normal physiological mechanisms to elevate temperature via the anterior hypothalamus, so reducing the difference.
Hence, sympathetic outflow is increased to cause more rapid temperature production by shivering and stimulation of the basal rate of metabolism. There is also vasoconstriction and piloerection. The individual has episodic sensations of feeling cold: classical chills.
Conversely, as the set point returns to normal after the end of the pathological stimulus, pyrexia resolves. However, the body is now too warm relative to its environment and sweating and vasodilatation occur.
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